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19 Charcot Foot: Surgical Management andReconstruction
241
[28]. Lateral column involvement was identied
by a decrease in the cuboid height, decreased calcaneal pitch, and decreased lateral calcaneal fth
metatarsal angle. Meyr and Sebag [29] recommended against using a single radiographic
parameter to predict midfoot ulceration because
of signicant positive and negative correlations
among various angles that could be measured.
Given that limitation, excellent reliability for
radiographic measurement of cuboid height on
subjects with midfoot Charcot neuroarthropathy
has been reported [30].
CT scans provide improved osseous visualization and can identify bone loss and dislocations
not seen on radiographs. MRI can identify bone
injury beyond the suspected area of Charcot as
evidenced by increased signal. MRI can also be
useful in cases of suspected osteomyelitis in
patients with active or healed wounds as well as
following the course of CN.
Nuclear medicine can also be helpful in the
evaluation of suspected for infected CN by labeling Leukocytes with either (99m)Tc-HMPAO or
(111)In-oxine [31]. In experienced centers accuracy in detecting bone infection can be greater
than 95%. Another benet is that white cell
labeled scans may be able to differentiate soft tissue infection versus aseptic inammation.
Single-photon emission computed tomography/
computed tomography (SPECT/CT) and bone
marrow scanning can also improve anatomic resolution of the foot and ankle [31].
Preoperative Evaluation
Patients with CN often have multiple comorbidities that can increase the perioperative risks of
surgery to include cardiovascular disease (hypertension, coronary artery disease, compensated or
uncompensated heart failure), diabetic nephropathy or autonomic neuropathy, poorly controlled
diabetes, and tobacco use. A thorough preoperative evaluation can predict the risk [32].
Patients undergoing Charcot reconstruction
benet from a structured multidisciplinary evaluation prior to the procedure. At King’s College
Hospital diabetic foot unit, the preoperative
assessment is commenced during their visit to a
dedicated “Foot School Clinic” (see gure). The
group of patients undergoing Charcot reconstruction procedures are seen along with their personal
care providers or family members in the clinic.
Detailed and interactive audio-visual presentations are made to the attendees by the members
of the MDFT (physician, surgeon, podiatrist,
physiotherapist, and occupational therapist), covering the generic information on their perioperative care. This is followed by individual
assessment and counseling of each patient, separately, by each member of the MDFT.The physiotherapist provides the information on the
prehabilitation regime (PREHAB) whereas the
occupational therapist goes through the microenvironment setup at the patient’s residence and the
regimens used for postoperative mobilization due
to the limitation of weight-bearing. All routine
perioperative assessments and investigations are
completed at this stage.
Routine blood investigations, including CBC,
renal and liver proles, and inammatory markers (C-reactive protein, ESR, procalcitonin) will
provide adequate assessment of surgical tness.
Blood vitamin D levels are often low in this group
of patients and it is recommended to routinely
provide vitamin D replacement. In the presence
of raised inammatory markers, radiological features of osteomyelitis or a history of previous
infection in the Charcot affected region, it is
advisable to perform bone biopsies for a denitive diagnosis and microbiological sensitivities.
Bone biopsy can be performed as an outpatient procedure in most patients. The patient
should be off antibiotics for at least 2weeks prior
to the biopsy procedure. The location of the bone
biopsy target material is determined based on the
imaging studies. Local anesthetic inltration can
be applied to the area of skin penetration if the
skin sensation is intact. Using aseptic technique,
the assembled trocar and cannula of the biopsy
instrument is pierced into adequate depth and in
the direction based on imaging studies. If an ulcer
is present, the biopsy entry point is chosen about
1cm away from the edge of the ulcer, avoiding
areas of active inammation. Using a standard
bone core biopsy technique, the specimen is har-
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D. K. Wukich and V. Kavarthapu
vested and sent for microbiology (culture and
sensitivities) and histological studies.
Vascular studies are routinely considered prior
to Charcot reconstruction, to rule out any signicant vascular compromise. If identied, this is
best addressed by performing the revascularization procedure about 4–6 weeks prior to the
deformity correction. The method of
revascularization is beyond the scope of this
chapter and will be discussed in other chapters.
Charcot Bone
Surgeons should recognize that bone is a dynamic
organ, and in normal homeostasis, bone resorption and bone formation are in relative balance. It
is well recognized that during the active phase of
Charcot neuroarthropathy, circulating osteoclasts
are signicantly elevated and metabolically
active resulting in a net loss of bone. Osteoclasts
also express inammatory cytokines such as
interleukin-1 beta, interleukin- 6, and TNF alpha
which facilitate the recruitment, proliferation,
and differentiation of osteoclasts. A histopathological and immunohistochemistry study of bone
retrieved from patients undergoing Charcot
reconstruction demonstrated that even though
patients were beyond Eichenholtz stage 1 (active)
and in the remodeling phase, expression of proinammatory cytokines was still present on pathological examination [33]. This nding has
implications in planning surgical reconstruction.
Surgeons planning to reconstruct Charcot
neuroarthropathy should have an understanding
of the quality of the involved bone. Herbst at al.
[34] classied the bone injury pattern as either a
fracture, dislocation, or fracture dislocation.
Bone mineral density was measured in the contralateral femoral neck or contralateral distal
radius, and not measured in the involved foot.
The authors found that patients who presented
with a fracture pattern had signicantly lowered
T-scores in bone mineral density compared to the
dislocation group. In fact, the age adjusted odds
ratio of a patient with osteopenia according to the
World Health Organization criteria as having a
fracture rather than dislocation was 9.5.
Dislocations and fracture dislocations had normal bone mineral density as measured in their
study. The fracture pattern was more likely to be
seen in the ankle and foot, while the midfoot
mostly involved dislocations. The hindfoot was
represented by fractures, dislocations, and fracture dislocations. The authors opined that the
osteopenia seen in the fracture group was not a
result of regional Charcot neuroarthropathy,
because the decreased bone mineral density was
observed in the contralateral extremities. They
further stated that the success of midfoot reconstruction may be related to the fact that the dislocation pattern has more of a normal bone mineral
density compared to the fracture pattern.
Limitations of this article included few patients
in the combination fracture dislocation group and
inclusion of patients presenting at different
Eichenholtz stages of the disease. Nonetheless
this study highlights an important point, namely
that identication of peripheral osteopenia may
be a potentially modiable systemic risk factor in
patients with diabetes and neuropathy.
Petrova at al. [35] studied 36 consecutive
patients who were treated for acute Charcot neuroarthropathy. They measured bone mineral density of the calcaneus from the involved foot and
compared it to bone mineral density from the
contralateral uninvolved foot. The authors found
that the bone mineral density of the involved foot
was signicantly decreased when compared to
the contralateral foot at presentation, after
3 months of casting and at clinical resolution.
There was a signicant decrease in bone mineral
density from the time of presentation until the
time of casting at 3months. After 3months no
signicant further decrease in bone mineral density occurred. Contrary to the opinions of Herbst
etal. [34], the authors felt that this reduced ipsilateral bone mineral density was secondary to
proinammatory induced osteolysis.
Greenhagen et al. [36] prospectively studied
central (core) and peripheral bone mineral density in a cohort of diabetic and non-patients.
Peripheral bone density was measured in the calcaneus of the extremity affected by CN, while the
19 Charcot Foot: Surgical Management andReconstruction
243
core bone density was measured in the lumbar
spine. The diabetic cohort was comprised of two
groups, one who had Charcot neuroarthropathy
and a control of diabetes patients without
Charcot. The bone mineral density of the Charcot
group was signicantly lower in the calcaneus
compared to the control group, and there was a
strong trend that the Charcot group bone quality
was lower than the diabetic control group
(p = 0.08). Interestingly the core bone mineral
density as measured in the lumbar spine was not
signicantly different between the three groups.
It is important to recognize that tools that
measure BMD are quantitative in nature and do
not measure the qualitative aspect of bone.
Patients with diabetes are at risk for fragility fractures due to decreased bone material strength
even in the setting of normal BMD [37]. This
increased risk of fracture is secondary to greater
cortical porosity, smaller cortical area, and
decreased bone strength. The implication in
Charcot patients is the obvious potential for stress
fractures even without observed trauma. Given
the alteration in bone remodeling and turnover
seen in diabetic bone, healing after arthrodesis
could be impacted as well due to decreased bone
quality and reduced biomechanical properties.
It has also been demonstrated that inammatory and bone turnover markers and acute Charcot
neuroarthropathy are elevated in peripheral
serum [38]. Inammatory markers such as
C-reactive protein, TNF alpha, and interleukin-6
were found to be signicantly higher in patients
with Charcot neuroarthropathy when compared
to diabetic patients without Charcot neuroarthropathy. Markers of bone turnover such as
C-terminal telopeptide, bone alkaline phosphatase, and osteoprotegerin were also signicantly
elevated at presentation. TNF alpha and interleukin- 6 declined signicantly after 3 months of
casting but did not change during the resolution
phase. Markers of bone turnover did not decline
signicantly after 3months of casting or at nal
resolution. Surgeons should recognize that the
potential for ongoing bone remodeling can occur
regardless of the timing of surgical intervention,
even after resolution of Eichenholtz Stage 1.
Indications forSurgery
Traditionally the indications for surgical intervention include:
• Non-braceable deformities
• Instability
• Impending ulceration of the skin
• Non-healing ulcers
• Recurrent ulcers
• Osteomyelitis of the midfoot, hindfoot, and
ankle
• Pain
Although symptomatic pain is relatively
uncommon, a subset of patients with Charcot
neuroarthropathy will complain of signicant
pain due to instability and deformity. Some
patients complain of difculty ambulating with a
rocker bottom deformity. Patients whose foot is
non-plantigrade are at high risk of ulceration. For
the purposes of this chapter, a non-plantigrade
foot/ankle is dened as one in which the patient
is bearing weight on skin that is not meant to bear
weight. For example, the plantar arch, lateral and
medial borders of the foot dorsal to glabrous skin
and skin over the medial and lateral malleoli are
not designed to bear weight. Midfoot CN commonly results in collapse of the arch with potential skin compromise medially or laterally on the
plantar surface. Collapse of the medial column
can involve subluxation/dislocation of the talonavicular, naviculocuneiform, or tarsometatarsal
joints. Laterally, the prominence is typically a
result of subluxation or dislocation of the
calcaneo- cuboid joint. Hindfoot and ankle deformities can result in signicant varus or valgus
malalignment that jeopardizes non-plantar skin
(see gure). Final surgical planning and goals of
surgery are best discussed by the multidisciplinary team, taking into consideration the factors that have been previously reviewed. While
each Charcot case is unique, reconstruction
should follow a logical and reproducible plan.
We recognize that customization of the approach
may be necessary, but in general the following
principles guide reconstruction.
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1. Perioperative medical optimization measures. A high portion of patients are on anticoagulation treatment and it is often not safe
to stop this medication preoperatively.
2. The choice of anesthesia: Peripheral nerve
block for pain relief is not considered in most
patients, due to the degree of sensory neuropathy. Tranexamic acid administration during induction is usually considered in most
patients.
3. Decision on the usage of tourniquet: This
is based on the vascular status and previous
revascularization procedures. It should be
recognized that many patients have medial
artery calcinosis that can prevent occlusion with a tourniquet, resulting in a venous
tourniquet.
4. Prophylactic antibiotics administration: This
is delayed until the intraoperative bone and
deep tissue samples are harvested.
5. Surgical approaches: The location of the
surgical approaches and their effect on the
vascular supply to the soft tissue envelope
and bones is discussed. It is preferred to
perform the reconstruction using one main
surgical approach, supplemented with additional small approaches as required. Foot and
ankle surgeons must be comfortable with a
360-degree approach to the pathology, as
many patients have compromised skin from
previous surgery.
6. Soft tissue releases: The associated soft tissue contractures are assessed, and plans are
made for lengthening or release for deformity correction. Commonly performed
soft tissue lengthenings in Charcot surgery
include Achilles (sagittal plane), posterior
tibial (varus deformities), and peroneal (valgus deformities).
7. Bone corrections: The location of the bone
osteotomies and the size of the bone wedge/
rhomboid resections are discussed based on
the assessment of clinical deformity (shape
and exibility) and imaging studies. CT
imaging with 3D reconstruction, weightbearing CT, and 3D printed model of the
bone deformity of the foot are useful tools
used for this assessment.
8. The xation devices: Due to the presence
of signicant bone loss, Charcot foot reconstruction procedures often require a combination of xation devices to achieve a
long-segment and rigid xation construct.
Hindfoot nail xation may require additional
cannulated screw xation across the hindfoot, and midfoot beams may require supplementary locking plate xation, to enhance
the rotational rigidity to the construct.
9. Wound closure: On occasions, it may not
be possible to achieve tension-free primary wound closure, particularly when the
degree of the deformity is severe or if concomitant ulcer debridement was done. The
need for performing a local rotational ap
or other appropriate plastic surgical procedure or usage of NWPT is anticipated. Soft
tissue complications are common, and one
method of minimizing these complications
is to approach the deformity from the convex side. Once the deformity is corrected, the
convex side is no longer under tension while
the concave side is subjected to tension.
10. Antibiotic regimen: In the presence of an
ulcer or previous history of infection, a biodegradable, osseoconductive and local antibiotic eluting calcium sulfate preparation can
be used to ll the bone voids and achieve high
concentrations of the antibiotic. The postoperative antibiotic regimen can be based on
the preoperative bone biopsy microbiology
sensitivities and modied according to the
sensitivities of intraoperative specimens.
11. Mobility: Postoperative weight-bearing status and the duration is determined based on
the complexity of the reconstruction procedure. Consideration is given on the status of
the opposite foot, as excessive load bearing
carries a risk of activation or re-activation of
Charcot changes in this foot.
Exostectomy
Several retrospective case series have described
medial or lateral exostectomy to decompress
bony deformities of CN and promote healing of
19 Charcot Foot: Surgical Management andReconstruction
245
recalcitrant ulcers [39–44]. Advocates of exostectomy cite high healing rates of ulcers; however, Catanzariti et al. [40] reported higher
success with medial column exostectomy versus
lateral column exostectomy. Molines-Barroso
etal. [42] found that sagittal plane radiographic
measures worsened after lateral column exostectomy as manifested by a signicantly decreased
calcaneal inclination angle and signicantly
increased talar declination angle.
Plantar ulcers due to bone prominence that do
not respond to surgical debridement can be considered for exostectomy. The infected ulcer is
excised, removing all infected and necrotic tissue,
down to the bone prominence. Any associated
tendon contractures, particularly of the Achilles
tendon is released or lengthened. The area of
bone resection is identied by careful palpation
and under the guidance of uoroscopy. All bone
prominence is excised completely using an oscillating saw or a sharp osteotome. If there are any
areas of residual bone necrosis or bone changes
consistent with osteomyelitis, the resection is
continued until all these areas are removed. Care
is taken not to leave any bone projections or loose
bone fragments as this will interfere with ulcer
healing. Where available, antibiotic loaded calcium sulfate preparation can be inserted into drill
hole channels created in the exposed bone as an
injectable form or applied on the bone surface as
beads (see gure). Local elution of high concentrations of antibiotic can potentially eradicate any
residual infection. The foot is examined after completion exostectomy for the presence of instability
due to bone resection. This requires a temporary
stabilization of this area with threaded wires or an
external xator for the duration of bone healing.
The open wound is managed either with a local
rotation ap, free ap, or negative pressure wound
therapy and appropriate ofoading.
Reconstruction ofActive
CharcotFoot
Acute (active) CN of foot normally responds to
immediate ofoading in a total contact cast
(TCC) or a well-tting brace until it reaches an
inactive phase. Despite adequate ofoading some
Charcot deformities continue to progress secondary to the degree of bone fragmentation or joint
dislocations. Progressive deformities make the
foot and ankle vulnerable to friction and shear
forces which can lead to ulceration. If the foot is
at risk of ulceration, and consequently infection
due to the presence of marked deformity and or
instability, it is advisable to perform surgical
reconstruction in the active phase of the disease.
Although ideally performed after resolution of
foot swelling and normalization of local warmth,
the degree and location of deformity may accelerate the surgical plan despite the presence of
active inammation. The use of a preoperative
compression dressing incorporating cast padding
in conjunction with elevation can result in substantial reduction in edema. The reconstruction is
performed using internal or external xation,
using the principles described later in this
chapter.
Reconstruction ofInactive
Charcotfoot
Severe Charcot deformity carries a high risk of
developing ulceration even with adequate
ofoading. Associated instability, often noticed
in severely affected feet due to non-union of bone
fragments effected by the Charcot process, provides additional challenge in preventing a skin
breakdown. Ulceration often progresses to developing infection and a chain of events resulting in
a major amputation. An ulcerated Charcot foot is
12 times more vulnerable to undergo a major
lower limb amputation [45]. Due to the high rate
of mortality following a major lower limb amputation in the diabetic population, a functional
limb salvage of Charcot foot can potentially save
the life of some of these patients.
The aim of Charcot foot reconstruction is to
achieve a plantigrade and stable foot that is infection and ulcer free and allows full weight-bearing
in a modied shoe or a brace. The incidence of nonunion following Charcot foot reconstructions is
high, and in general a stable non-union or pseudoarthrosis has been considered as an acceptable out-
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D. K. Wukich and V. Kavarthapu
come. Some brous non-unions achieve adequate
stability and are still desirable; however, mobile and
unstable non-unions should be avoided in a neuropathic foot, as this can result in recurrence of deformity over a period of time. Ideally, the surgical aim
should be to achieve a full bone fusion or a stable
brous union in every procedure.
Deformity Correction
Charcot foot and ankle deformity correction is
achieved by achieving adequate soft tissue balance,
through release or lengthening of contracted tendons and other soft tissues, and performing wedge
or rhomboid bone resections on the convexity of
the deformity, based on surgical planning. The
choice of incision and surgical approach depends
on the location of the deformity and the vascular
status of the angiosomes. Multiple major surgical
incisions should be avoided as they carry a signicant risk of wound breakdown and infection.
Careful deep dissection of the incisions developing thick and deep soft tissue aps and protecting
vascular structures is critical. All joints intended
for bone fusion are exposed and thoroughly prepared. Following the desired deformity correction,
stabilization of the correction is achieved by using
either internal or external xation methods. Recent
systematic review studies revealed no signicant
advantage of one method over the other (see gure) [46]. With the recent introduction of Charcotspecic internal xation devices, there has been a
recent increase in the usage of this internal xation
method for reconstructions.
Hindfoot andMidfoot Stabilization
Using Internal Fixation
The surgical principles for Charcot foot and ankle
internal xation method have evolved since
Sammarco et al. [47] described a decade ago,
when the term “Super-construct” was introduced
for this xation. This advocated extension of
bone xation beyond the zone of injury, the usage
of the strongest xation device that is tolerated
by the soft tissue envelope and application of the
xation devices in a novel position that maximizes its mechanical function. Subsequent studies identied the additional need for the xation
construct to provide rigidity against axial, bending, and rotational forces to improve the xation
outcomes. The current established principle of
internal xation for Charcot reconstruction is
“durable long-segment rigid xation with optimal bone opposition.”
Hindfoot Internal Fixation
An intramedullary hindfoot nail (IMHN) is
the most accepted method of internal xation for Charcot hindfoot reconstruction.
Biomechanically, IMHN is a load sharing device,
provides better mechanical environment, and
has higher bending and torsional stiffness compared to other forms of internal xation. It can
also provide intraoperative compression of the
bone fragments over the nail and that results in
optimal bone opposition. The torsional rigidity of
the construct may be suboptimal in the presence
of marked bone loss and may require additional
xation (see gure) [18].
A trans-bular lateral approach provides good
access to the ankle and subtalar joints for preparation and wedge resections and is the most common surgical approach. Alternative approaches
may be considered for severe valgus deformities
or those with compromised lateral soft tissues.
Following the soft tissue releases and bone resections, the hindfoot is stabilized temporarily with
2mm Kirshner wires, to maintain correction. The
entry point for the hindfoot nail is determined
under uoroscopy guidance and care is taken to
make sure that guide wire goes through the midportion of calcaneus. The intramedullary reaming to adequate diameter and depth is performed.
The Kirshner wires are then removed and the
chosen length and diameter hindfoot nail is
inserted, using the recommended standard surgical technique. Correct length and diameter of the
nail should be chosen to achieve a good isthmal
t of the nail is the tibial diaphysis. There are
varying opinions on whether to use short or long
retrograde nails, and IMHN sizes range from 150
19 Charcot Foot: Surgical Management andReconstruction
247
to 300 mm in length. Axial compression of the
bone fragments over the nail is attained before
inserting both proximal and distal locking screws.
In the presence of signicant bone loss or during
severe hindfoot correction that utilizes large bone
resections, optimal rotational rigidity cannot be
achieved with a standard hindfoot nail construct
alone. To enhance the rotational rigidity in such
constructs, an additional cannulated screw can be
inserted from calcaneum into distal tibia (see gure). Supplemental xation can also be achieved
with a locking plate spanning distal tibial and
talus.
Midfoot Internal Fixation
Charcot midfoot deformities generally fall into
one of three patterns:
1. rocker bottom forefoot abduction
2. dorsal subluxation/dislocation
3. forefoot adduction (see gure).
The rocker bottom forefoot abduction deformity is the commonest pattern and results from
the involvement of the medical column collapse.
Signicant deformity often results in marked
reduction of calcaneal pitch and contracture of
Achilles tendon. Sagittal plane deformity can be
quite signicant.
Midfoot deformity correction often requires
posterior muscle group lengthening to achieve
soft tissue balance in the sagittal plane. This can
be accomplished with required percutaneous
tendo Achilles lengthening, open Achilles tendon
lengthening, or gastrocnemius recession. This is
performed in conjunction with anatomic restoration by performing bone wedge resections on the
convex side. Most deformities are associated
with rocker bottom and forefoot abduction components. A medial midfoot approach allows performing a plantar and medial based bone wedge
resection, with the apex of the wedge placed in
the lateral part of the cuboid bone, thereby preserving the cuboid’s lateral cortex. This intact
lateral cortex of the cuboid allows controlled correction of the forefoot deformity by closing the
wedge and permits the application of tension
band plating principle for the medial column xation (see gure). The deformity correction can
be provisionally held with two or more 2 mm
Kirschner wires.
The deformity correction can be stabilized
with a medial column beam or locking plate or a
combination of these. For locking plate xation
technique, initial lag screw xation with one or
two cannulated lag screws across the osteotomy
is done before using a strong and low prole contoured locking plate spanning across the medial
column for neutralization. More recently an
intramedullary medial column beam spanning
the rst metatarsal and talus, inserted either retrograde through the metatarsal head or antegrade
through the posterior body of talus, is favored as
it provides excellent compressive xation and
requires smaller surgical approach. If any residual rotational instability is noted, this can be
enhanced by supplementing the xation with a
locking plate across the medial column (see gure). Most midfoot deformities, involving the
medial column, do not require a lateral column
xation, if the lateral cortex of cuboid is left
intact. However, for complex deformities, as
noted in some dorsal subluxation patterns and
those that involve medial and lateral column
rocker bottom deformity, additional lateral column xation is required. This can be achieved by
using additional lateral beams inserted from the
third and fourth metatarsal into calcaneus, along
with an additional plate xation spanning the
base of fourth metatarsal to the anterior part of
calcaneum, if required.
Two-Stage Reconstruction
Charcot foot reconstruction is typically carried out
as a one-stage procedure, even in the presence of a
non-infected ulcer. In the presence of an ulcer, thorough surgical debridement is performed at the
beginning of the procedure, followed by the reconstruction using the principles enumerated above.
Multiple bone and soft tissue specimens are collected during the procedure for microbiological
analysis and empirical antibiotic therapy is com-
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D. K. Wukich and V. Kavarthapu
menced until the microbiological sensitivity results
are obtained. The wound from ulcer debridement is
managed with primary closure, a local rotation ap,
or NPWT.In some cases, the ulcer wound can be
left open and healing occurs rapidly once the osseous deformity has been corrected.
Charcot foot deformity associated with an
infected ulcer or deep infection is best managed
as a two-stage procedure (to achieve functional
limb salvage) [48]. The rst stage of this treatment consists of surgical debridement of all
infected and necrotic tissues using the principles
described above. It is critical that multiple deep
tissue and bone specimens from the infected
areas are harvested for microbiological culture
and sensitivities. Infected bone and prominences
are thoroughly excised. In the presence of marked
deformity, osteotomy or wedge resection is done
to reduce deformity and decompress the soft tissues. The bone voids that are created from
debridement and osteotomy are lled with an
antibiotic impregnated calcium sulfate preparation, for local antibiotic elution in high concentration to eliminate any residual infection. The
choice of the antibiotic used in this preparation is
based on the previous microbiological sensitivities. If an osteotomy is done, the associated foot
instability is addressed with the application of
threaded guidewires or an external xator temporarily. The open wounds created from ulcer
debridement or surgical wounds are managed
with negative pressure wound therapy (NPWT).
Infection eradication is achieved by administering empirical intravenous antibiotics that are
changed to targeted antimicrobials once the intraoperative specimen microbiology results become
available. The duration of antibiotic administration is based on the improvement noted clinically
and serologically. After a period of 6–10 weeks
of interval treatment that includes advanced
wound care and foot ofoading, the second stage
of treatment is delivered.
The second stage of the reconstruction is typically done using the external xation option;
however, recent reports have shown good results
with internal xation methods using the principles described above (see gure). Repeat debridement of the previously infected areas and further
harvesting of deep tissue and bone samples are
done during the second stage, followed by soft
tissue releases if required, wedge bone resections, joint preparations, and internal xation
using the principle of “long segment and rigid
internal xation with optimal bone opposition,”
as described above. Gentamycin or Vancomycin
impregnated injectable calcium sulfate preparation (Cerament® G or V, Bonesupport, Lund,
Sweden) is applied to the bone voids and around
the osteotomy sites for local antibiotic elution.
Targeted intravenous antibiotics are continued
for 2–6weeks based on the improvements noted
clinically and serologically. The postoperative
care is similar to the one- stage reconstruction.
Postoperative Care
ofReconstructed Charcot Foot
The leg is elevated postoperatively to reduce
swelling and the patient mobilized non-weightbearing in a well-padded below-knee splint.
Closed surveillance of the surgical wound is
undertaken, and once the wound is stabilized, a
total contact cast is applied. Bivalving of the
TCC is especially helpful to facilitate regular
wound inspections. The patient is discharged
home, when safe mobility levels are reached,
non-weight-bearing in a TCC. Postoperative
radiographs are taken at 6 and 12 weeks and regularly then after as required. The non-weightbearing TCC is continued for at least 3months
post-surgery. Progression to partial weightbearing in the cast can be initiated once radiographs demonstrate signs of osseous healing.
Ultimately, progression to custom-made orthotics and/or shoes is fabricated to assist in independent ambulation. Some patients may benet
from additional stability by using a cane to help
mitigate the consequences of peripheral
neuropathy.
19 Charcot Foot: Surgical Management andReconstruction
249
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